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Article: Lipocalin-2 Exacerbates Lupus Nephritis by Promoting Th1 Cell Differentiation

TitleLipocalin-2 Exacerbates Lupus Nephritis by Promoting Th1 Cell Differentiation
Authors
Keywordslipocalin-2
lupus nephritis
Th1 cells
Issue Date2020
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org
Citation
Journal of the American Society of Nephrology, 2020, v. 31 n. 10, p. 2263-2277 How to Cite?
AbstractBackground: Lipocalin-2 (LCN2) is an indicator of the severity of lupus nephritis (LN) and plays a pivotal role in immune responses, but it is not known if its effect on LN pathogenesis derives from regulating the immune imbalance of T lymphocyte subsets. Methods: The expression of LCN2 in T cells and kidneys was assessed in renal biopsies from patients with LN. We investigated the relationship between LCN2 levels and development of LN and systemic illness by injecting anti-LCN2 antibodies into MRL/lpr mice and analyzing pristane-treated LCN2−/− mice. Results: LCN2 is highly expressed in CD4+ T cells and in renal tissues, and is associated with severe renal damage in patients with LN and in mice with experimental lupus. LCN2 promotes IFN-γ overexpression in CD4+ T cells through the IL-12/STAT4 pathway in an autocrine or paracrine manner. Both neutralization of LCN2 in MRL/lpr mice and genetic depletion of LCN2 in pristane-induced lupus mice greatly ameliorate nephritis. The frequency and number of splenic and renal Th1 cells decrease in proportion to LN disease activity. Conversely, administration of LCN2 exacerbates the disease with significantly higher renal activity scores and increased numbers of Th1 cells. Conclusions: LCN2 plays a crucial role in Th1 cell differentiation, and may present a potential therapeutic target for LN.
Persistent Identifierhttp://hdl.handle.net/10722/287761
ISSN
2020 Impact Factor: 10.121
2015 SCImago Journal Rankings: 4.699
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, W-
dc.contributor.authorLi, W-
dc.contributor.authorZhang, Z-
dc.contributor.authorTang, X-
dc.contributor.authorWu, S-
dc.contributor.authorYao, G-
dc.contributor.authorLi, K-
dc.contributor.authorWang, D-
dc.contributor.authorXu, Y-
dc.contributor.authorFeng, R-
dc.contributor.authorDuan, X-
dc.contributor.authorFan, X-
dc.contributor.authorLu, L-
dc.contributor.authorChen, W-
dc.contributor.authorLi, C-
dc.contributor.authorSun, L-
dc.date.accessioned2020-10-05T12:02:53Z-
dc.date.available2020-10-05T12:02:53Z-
dc.date.issued2020-
dc.identifier.citationJournal of the American Society of Nephrology, 2020, v. 31 n. 10, p. 2263-2277-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/287761-
dc.description.abstractBackground: Lipocalin-2 (LCN2) is an indicator of the severity of lupus nephritis (LN) and plays a pivotal role in immune responses, but it is not known if its effect on LN pathogenesis derives from regulating the immune imbalance of T lymphocyte subsets. Methods: The expression of LCN2 in T cells and kidneys was assessed in renal biopsies from patients with LN. We investigated the relationship between LCN2 levels and development of LN and systemic illness by injecting anti-LCN2 antibodies into MRL/lpr mice and analyzing pristane-treated LCN2−/− mice. Results: LCN2 is highly expressed in CD4+ T cells and in renal tissues, and is associated with severe renal damage in patients with LN and in mice with experimental lupus. LCN2 promotes IFN-γ overexpression in CD4+ T cells through the IL-12/STAT4 pathway in an autocrine or paracrine manner. Both neutralization of LCN2 in MRL/lpr mice and genetic depletion of LCN2 in pristane-induced lupus mice greatly ameliorate nephritis. The frequency and number of splenic and renal Th1 cells decrease in proportion to LN disease activity. Conversely, administration of LCN2 exacerbates the disease with significantly higher renal activity scores and increased numbers of Th1 cells. Conclusions: LCN2 plays a crucial role in Th1 cell differentiation, and may present a potential therapeutic target for LN.-
dc.languageeng-
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.subjectlipocalin-2-
dc.subjectlupus nephritis-
dc.subjectTh1 cells-
dc.titleLipocalin-2 Exacerbates Lupus Nephritis by Promoting Th1 Cell Differentiation-
dc.typeArticle-
dc.identifier.emailLu, L: liweilu@hku.hk-
dc.identifier.authorityLu, L=rp00477-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1681/ASN.2019090937-
dc.identifier.pmid32646856-
dc.identifier.pmcidPMC7609012-
dc.identifier.scopuseid_2-s2.0-85092250684-
dc.identifier.hkuros315187-
dc.identifier.volume31-
dc.identifier.issue10-
dc.identifier.spage2263-
dc.identifier.epage2277-
dc.identifier.eissn1533-3450-
dc.identifier.isiWOS:000577091000009-
dc.publisher.placeUnited States-
dc.identifier.issnl1046-6673-

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